Searching for the Essential Simplicity that underlies all complex subjects. Of my 168 posts (listed in 'Blog Archive') the currently most popular are automatically listed in the right hand column. Total Reads (To date: 46,819 hits)

Thursday, 30 November 2017

Thank you for the invitation to attend Andrea Leadsom's meeting on 8th December. I am currently in Mexico, and it would be impractical. Sorry.

My views:

(1) for complete separation, the task for the civil service seem essentially impossible inside 2 years. Five would be more realistic, or 10.

(2) a solution to the Irish border seem almost impossible, except that of UK staying inside an EU-compatible customs union.

(3) to maintain trading access to EU we must maintain EU standards, which in any case suit the British preference for safety, and the environment.

(4) we have already lost the medicines agency, and banking authority. We must clearly brace ourselves to lose remaining vestiges of influence in the world's second largest trading and cultural block as we press on out of the EU.

(5) I THEREFORE FAVOUR A NORWEGIAN TYPE RELATIONSHIP WHERE WE PAY WHAT IS NECESSARY TO RETAIN THE ACCESS WE NEED AND WANT. At least for 5 years.

Tuesday, 21 November 2017

I believe that M. Barnier has just put the crucial question in a concise form. Yesterday (20th November), Barnier said:

“The UK has chosen to leave the EU. Does it want to stay close to the European model or does it want to gradually move away from it? The UK’s reply to this question will be important and even decisive….”.

That is it in a nutshell. I want regulation and high standards. What do you want? What does Britain want?

that many Brexiters would be “very happy for the UK to become a regulatory satellite of the US”, while “some in the present cabinet barely know what a trade negotiation is, let alone why it is desirable”.

Sunday, 12 November 2017

Werner on GDP and Interest Rates

Lee and Werner have posted a paperdestined for the Journal of Ecological Economics in 2018. According to Lee and Werner there is essentially complete agreement amongst all schools of economic thought, that lower interest rates stimulate economic growth; they extrapolate to a belief that when the Bank of England lowers ‘Bank Rate’ (the overnight rate of interest at which it lends to commercial banks) it is trying to boost growth of the economy. Lee and Werner’s object is to test, against the data, whether low interest rates cause the economy to grow. Of course, they cannot show causation, but they can test whether or not a fall in interest rate precedes a rise in ‘growth’. Their answer is the complete opposite – not only does increased rate of ‘growth’ lead a change of interest rate (rather than lag it), but raised rate of ‘growth’ correlates with a raisedinterest rate (rather than a fall).

I propose to return to the question of how to determine the growth of the economy, but wish first to consider why the Bank of England tinkers with the base rate of interest on the overnight loans it offers to its commercial bank customers, which we call “Bank Rate” or “Base Rate”. Ostensibly ‘Friedmanite’ central banks such as the Bank of England (BoE) are tasked with maintaining the stability of the currency by controlling inflation at a steady rate of 2%. The Bank of England currently uses two methods to manipulate the purchasing power (in Britain) of the pound (i.e. the cost of the basket of goods in the Consumer Price Index). These are: [i] rate of interest charged on overnight loans from the Bank of England, and [ii] asset purchase (i.e. Quantitative Easing).

The idea behind the first is presumably the monetarist belief that the quantity of money in circulation directly affects prices; doubling the money will double the price of goods (and halve the value of the money). And of course, money nowadays is mostly credit, rather than coin. I have no idea what volume of business flows into and out of the BoE reserves every night, nor what a commercial bank would do if the BoE said “sorry, you cannot borrow from us this evening.” I imagine that Bank Rate is largely operating as a signal. If Bank rate rises, all the lenders in the country gleefully raise their rates. If the economy stagnates and the Governor fears a recession, he will signal a willingness to encourage lending by lowering base rate. However, when base rate is essentially zero he cannot use that tool to encourage inflation; he turns to Quantitative Easing.

The idea behind Quantitative Easing seems to be as follows. The Treasury issues gilt-edged IOUs at such an interest rate that they do not all get sold. The Bank of England buys (up to 70% of) them, so holding down longer-term interest rates. If the Bank of England buys these ‘assets’ from commercial banks these latter acquire (in exchange) money they can lend out, or reserves at the BoE they can use as surety against extending credit to smaller customers. You might ask where the BoE gets the money with which to buy the Gilts? But remember, it has the power to print notes; so it (therefore) does not need to; it simply gives the liquid asset of digital cash in exchange for the gilt-edged IOU; it can always swap it back again. In many ways QE is simply doing, for longer-term interest rates, what the BoE routinely does for its overnight Bank Rate. But the process injects ‘broad money’ (in the form of credit) into circulation, and that can cause inflation if it gets into the hands of the general public. There can be a delay, of months or years, depending on what the commercial banks do with their new money (sit on it or lend it out); and on whether the general public borrow that money to build factories or fund purchases. But it will eventually cause inflation, unless the BoE swaps back the IOUs it purchased.

For two centuries Britain has watched the economies of other countries grow faster than its own. This growth represents capital accumulation and in its early phase is logarithmic (auto-catalytic). It is usually measured as gross domestic production (GDP), which is a compilation of all the incomes of all the people in an economy, expressed in the local currency. If we do not grow as fast as our competitors we loose market share; and we cannot grow as fast because we are no longer in the logarithmic phase of growth.

Because nominal GDP is expressed in local currency, it reflects not just accumulation of capital, but also inflation. Let us consider a peculiarly simple but quite plausible form of inflation in which, at the beginning of every financial year, all prices and all wages rise abruptly by 5%. The citizens and businesses would be no better off; nor worse off. A bag of flour would cost 105% of what it did the previous year, but citizens would soon realise that their salary would stretch exactly as far as before. At the end of the year the macroeconomists would note a 5% jump in nominal GDP, but this is not growth – except to ‘the media’. Any sensible discussion of GDP must start by correcting nominal GDP for the change in value of the currency (using e.g. RPI or CPI). (See also my post on Growth; and on Coppola Comment.)

Let us now look at the data of Lee and Werner. They plot the “year-on-year growth” in nominal GDP over a period of 50 years from 1960, presumably taking the published GDP for each 3-month interval and subtracting that of 12-months before (thereby introducing a 6-month offset into the profile; any growth in the 12 months to December 1970 being ascribed to December 1970 and not to June 1970). On the same graph they plot interest rates on 3-month Treasury bills or (on another graph) 10-year government bonds. These interest rates are not simply base rate, but are complex reflections of (a) instantaneous base rate, (b) what the markets think will happen to base rate and (c) what the markets think will happen to inflation over the period of the loan.

My interpretation of their data is that in all 4 major economies the rate of inflation rises and falls irregularly (but with a tendency towards a 5-7 year periodicity) over the 50 years of the study, causing a similar fluctuation in nominal GDP, and (with a slight lag) the 3-month and 10-year interest rates. Lags are the essence of the over-shoots and under-shoots of the business cycle. If information were instantly available to businesses and bankers, and if the spreading of rumours and building of factories were instantaneous, there would be no business cycle.

(It would be interesting to compare, for each time-point, (i) the 3-month rate, (ii) 10-year rate, (iii) base rate, (iv) inflation rate, and (v) ‘corrected’ GDP growth-rate ascribable to that time-point; but that was not done.)

++++++++++++++++++++++++++++

‡‡ There are old men in pubs remembering when beer was 20p a pint and their fist car cost £600. In 1970 the average house cost £4975 and the average annual wage was £5700 [http://www.independent.co.uk/news/uk/this-britain/1970-vs-2010-40-years-when-we-got-older-richer-and-fatter-2017240.html; https://www.theguardian.com/uk/2004/mar/05/health.drugsandalcohol]. So in 1970 the annual wage was equivalent to 28,500 beers or 9.5 cars, or 1.1 houses. Today our average annual wage of £25,000 is equivalent to 8,000 beers or 2.5 average cars, or 0.11 average houses. But these figures do not capture the whole picture, or you might think we were considerably worse off now than in 1970. We work less, live longer, fly to the sunshine for our holidays. We throw away worn clothes and broken umbrellas, and play with our smartphones in front of our flat-screen TVs. I have not met anyone who would prefer 1970 to 2017. Nor would I, even if it meant being young again – I think.

;

★★ If the real (i.e. corrected) GDP of Britain increased 5% on the previous year, what has increased? To simplify, it could be the population, leaving us identically well off on a per caput basis; or we could all work longer days; or (finally) it could be that a new machine makes 110 shirts per diem instead of a mere 100. That new machine could be bought on credit if interest rates were temptingly low. Believing that is easy; proving it is hard.

Tuesday, 7 November 2017

I like the George Nathan quote, painted on the wall by the fruit machine: "I drink to make other people interesting". So true. I had 2 pints today which is most unusual, and we had some enjoyable conversation. 'H' had been woken by his hot-water system, John was furious with an electrician who wanted to charge 10 times the list price for a replacement wireless thermostat. John and I talked, as is usual, about aspects of safety in the London underground, the explosive properties of warm dusty air, and such. Attention turned to the Mail's Quick Crossword where there was one remaining clue:

2. (down) — Toxophilite (6), A-C-E-,

I suggested ARCHER, to general amazement. Barry said he knew that fletchers made arrows, which seemed to me a golden opportunity to remind everyone of the Fletcher's trolly, as an ingenious way to neutralise friction and study gravity. That prompted Barry to ask the Speed of Gravity, a pretty big leap if you ask me; perhaps it was something that was bothering him. 'H' suggested it was 9.81 m/s, but we quickly persuaded him that his was the acceleration of something due to gravity (in one second), and not of gravity itself. John said he thought it was something to do with the warping of space-time, to which I nodded, but I could not think how to follow that up, so I proposed the experiment of rapidly producing a mass here and seeing how quickly you could feel its effect over there. I remembered the Schiehallion experiment, where someone climbed Mt. Schiehallion with a pendulum, to "weigh the mountain". I suggested that gravity would travel at the speed of light. Wikipedia seemed to concur. I think we were all pretty impressed with ourselves. Someone hoped that Einstein would have been flattered had he dropped in, and another agreed that we seldom reached such philosophical heights in the New Inn. I drained my glass. John offered me another but I declined and picked up my watering can as I made for the door, causing another guffaw from my merry companions: "Why did so few chaps carry watering cans these days?" etc. Good place, the New Inn.

Thursday, 26 October 2017

Shostak on 'The Importance of Theory'.

“The purpose of a theory is to enable to ascertain the definition of a phenomenon that is subject to investigation. The correct definition attempts to identify the essence of the phenomenon i.e. the key parts that drives the phenomenon. For instance, the definition of human action is not that people are engaged in all sorts of activities, but that they are engaged in purposeful activities – it is purpose that gives rise to an action. So when Tarullo states that Fed policy makers do not know the causes that drive inflation he basically says that Fed policy makers have not as yet established the correct definition of inflation. Is it then valid to be practical, as suggested by Tarullo, to focus only on the data to understand what inflation is all about? If Fed policy makers respond to changes in price indices without establishing what drives these changes this runs the risk of making things much worse.”

My literal translation (into English).

The reason for propounding a theory is to make possible the definition of the phenomenon under investigation. A correct definition identifies the essence of the phenomenon, i.e. the forces that drive the phenomenon. For instance, the correct definition of “human action” indicates that activities are purposeful, not merely varied; for it is the purpose that gives rise to the action.So, when Tarullo states that policy makers at the Federal Reserve do not know the causes that drive inflation, that is tantamount to saying that they have the wrong definition of inflation. Is it then valid to focus only on the data (as a means of understanding the ‘meaning’ of inflation)? To react to change in the Consumer Price Index without understanding what is causing those changes could make matters worse.

My Comment

I do not think the reason for propounding a theory is the one given, and I disagree with Shostak’s definition of “definition”, and (in addition) his definition of “human action”. But this nonsense is not germane, and perhaps can be safely ignored. I agree with Shostak that the Federal Reserve should try to understand the cause (or causes) of any current inflation. It may be that inflation indicates that something is changing; the volume of money, or of goods. An intelligent Government would try to identify what exactly is changing, and adjust for that. They should not merely obliterate the signal. There is a parallel in healthcare. Pain is a signal of something going wrong. An analgesic like paracetamol obliterates the signal but does nothing to identify precisely what is going wrong, and nothing to rectify the problem.Dr. Shostak is angry about inflation because it robs value from those with positive bank balances. But there will (presumably) be others who like inflation because it gives value to those with negative balances, and those who create the money. But let us get back to the "importance of definition". Dr. Shostak writes:

"However, if we accept that inflation is about rises in money supply and not a rise in prices then all ........ can be easily explained. It is not the symptoms of a disease but rather the disease itself that causes the physical damage. Likewise it is not a general rise in prices but rises in money supply that inflicts the physical damage on wealth generators."

Once again I disagree. I believe that the money supply should increase as and when necessary, for example, when there is an increase in goods. But there is a quite different, and much more subtle argument in favour of a controlled low level (2%p.a.) of inflation. Is the Keynesian position not generally accepted that, for psychological reasons, an economy is more stable and more easily controlled when there is a constantlow level of inflation? Do we throw out the "General Theory" and 8 decades of largely successful government for the sake of simple mathematics? I do not think the case is made, yet. Maybe we could agree that, as a type of covert taxation, inflation is a bit underhand.

Monday, 23 October 2017

Predictable, effort-related, chest pain is called stable angina. The consensus view is that ‘diseased’ (or atherosclerotic) arteries, partly occluded with cholesterol-rich plaques, require raised blood pressure, so more effort is required from the heart. If the coronary arteries supplying the heart muscle are healthy, blood pressure would rise, and in time ventricular hypertrophy would be evident. But if they are themselves partially occluded, part of the heart muscle becomes inadequately oxygenated when under this increased work load; this ischaemia causes pain — in the myocardium (and referred areas such as: neck, jaw, shoulder, or arm).

There are two main coronary arteries, but they branch and fuse, and there is considerable variation between individuals. Occlusion can occur in one, or more limbs, and can, in time, cause the vascular network to adapt. When 130 patients with chest pain syndromes were examined for physical evidence of coronary artery disease 93 patients showed positive, but 37 showed no sign of disease [1]. I understand that ischaemia in a small part of the heart can be as painful as in a large part. So it is possible that the physical tests for occlusion were not sufficiently discriminating. But it is also stressed that not every chest pain shows the effort-induced aetiology of stable angina. A very similar pain can be caused by emotional stress, where the transient cardiac ischaemia presumably results from adrenaline stimulating β1 receptors, which results in increased cardiac effort (and oxygen-demand) by increasing heart rate, conduction velocity, and stroke volume. According to one source [2], in about 2% of people with angina, the closure of the artery (or arteriole) is due to “coronary artery spasm”. According to another source [3] this aetiologiy is 5 times more common in women than men.

One question that nags me is as follows: Does the pain experienced during exercise coincide with (and thus 'flag') further damage occurring to the coronary vessels? There seem to be two ways in which this might be the case.

The pain (ex hypothesi) indicates ischaemia, which in turn can cause cell-death (when the cells are unprepared). Dead cells may lead to scar tissue and possible foci for plaque build-up.

Ischaemia can cause cells to generate superoxide radicals, which can modify lipids (including cholesterol), or can react with nitric oxide to form peroxynitrite. Peroxynitrite can nitrate protein tyrosines. The presence of antibodies against nitrotyrosine in patients with atherosclerosis, myocardial ischemia, have confirmed the occurrence of such nitration. [4]

This question is important, because the patient will want to know whether to exercise as much as possible, or to avoid (as much as possible) the pain of over-exertion.

Sunday, 15 October 2017

I find stressful, and begin to resent, the shilly-shallying on the Brexit negotiations. Here is a simplifying suggestion. Britain has offered to honour commitments made during membership. Barnier wants to know how much that is. Why not everything that we were paying before the brexit referendum? But during the transition period, we receive all the benefits that we received as a full member before the referendum. (No more closed-door stuff.) At least we know how much that was, and that we can afford it; and we know that it is regarded as value for money by 48% of Britons. During the transition period we enter no new commitments, and we pull out, one by one, from the costs and the privileges of membership. The transition ends when the negotiations end. They might take decades. Yours sincerely, Ian West--Ian West, 9 Thenford road, Middleton Cheney, Banbury, OX17 2NB. (Tel: 01295 713889; mob: 07906 750986)

Friday, 13 October 2017

“Coppola Comment” Comment

Growth:

Like organisms, I believe economies can grow until they approach maturity, when they will enter a ‘steady-state’. It is neither possible nor desirable to grow for ever. By the way, GDP cannot be used as a measure of growth unless corrected for devaluation. True growth (in wealth) would have to involve either an increase in population or productivity (per worker), or both. I cannot see why anyone should want a mature economy to grow. No sane Briton could want an increase in the population (of Britain), nor an increase in the ratio of concrete to green-space, in Britain. There will (in Britain) be even less interest in the growth of economies elsewhere in the world.

Inflation:

I suppose inflation is (in essence) the willingness of some people (sufficient people) inside a currency zone to pay more for a standard item (or sufficient basket of items). And I suppose this could happen if the items become more scarce, or if the currency becomes more plentiful.

I assume that the conventional aim of 2% inflation depends entirely on politics and psychology; not on economics. People are unwilling to accept a lowering of money wages. If government wishes to lower real wages (for whatever reason), that can be achieved most easily by fixing money wages and waiting for inflation (devaluation). In Japan, with a mature and stable economy, I cannot see why anyone could possibly want inflation, whether in the form of devaluation, or of growth. (If Japan wanted inflation, I think that could be achieved, with a printing press.)

Interest Rates:

‘The natural rate of interest, also called the long-run equilibrium interest rate or neutral real rate, is the rate that would keep the economy operating at full employment and stable inflation’.” When base interest rate was the only lever the Central Bank could pull, the Olson and Wessel definition probably made some sense; the central bankers spent their time sliding the lever up and down while watching their two indicators of success. Quantitive easing provides another lever for the Central Bank, and doubtless upsets the theory of ‘natural interest rate’. Even without the complication of quantitative easing, it seems quite possible that the concept of Natural Interest Rate contains internal contradictions: [a] Full employment may not be ‘natural’. [b] Full employment, when achieved, might not be compatible with the interest rate required for stable inflation (unless stable inflation is used to provide a definition of “full employment”).

Coppola clearly knows all that, and in her blog is not so much dismayed, as laughing at the discomfort of the economists who were armed not with basic principles but with rules of thumb.

Tuesday, 10 October 2017

Angina — Some Questions

The heart must deliver oxygenated blood to (inter alia) the brain, skeletal muscle and the heart muscle itself. Exercise increases the oxygen requirement of the skeletal muscles, and the heart pumps harder. That increased effort, in its turn, increases the oxygen requirement of the heart muscle. The consensus view is that ‘diseased’ (or atherosclerotic) arteries, partly occluded with cholesterol-rich plaques, require raised blood pressure, so more effort is required from the heart. If the coronary arteries supplying the heart muscle are healthy, blood pressure would rise, and in time ventricular hypertrophy would be evident. But if they are themselves diseased (>69% occluded), the heart muscle becomes inadequately oxygenated when under this increased work load; this ischaemia causes pain — in the myocardium (and referred areas). This predictable, effort-related, chest pain is called stable angina. (A very similar pain can be caused by emotional stress, where the transient cardiac ischaemia is presumably the result of vaso-constriction caused by adrenaline and the ’stress-response’; a significantly different mechanism.)

Cause of Pain

Note that ischaemia in the brain causes fainting, but not pain. Ischaemia in the legs might be expected to cause pain there, or at the very least weakness but, by some mechanism, the legs keep working and it is the heart muscle (which also keeps working) that experiences pain. The biochemistry causing the pain is still mysterious but may involve adenosine, and possibly ATP [1].

Cause of Sclerosis

If you ask what ‘causes’ the atherosclerotic obstruction the answer given is indistinct. The literature will tell you that the major (modifiable) risk factors for cardiovascular disease are [2]:

But Risk Factors do not in general cause anything; they merely correlate, they are markers. Amongst them there may be one 'cause' that causes all the rest. Or the 'cause' may still elude detection. It is said that these risk factors interact, either additively, or possibly even synergistically [3]. But they are clearly linked. For example, it is easy to see that narrowed arteries might necessitate raised blood pressure; but it is harder to see how raised blood pressure could directly cause narrowing of arteries; bloating rather.

It is hard to see from this list what mechanism really ‘causes’ atherosclerosis. There are two theories; one is called the “reverse cholesterol transport’” hypothesis, the second theory involves lipid oxidation.

Evidence for the Reverse Cholesterol Transport hypothesis [3] comes from finding that unloaded HDL apoproteins, capable of binding cholesterol, is protective. So also is contriving (by gene-therapy) to raise circulating levels of various of the protein components of HDL such as apoE and apoA [5].

The Oxidised Lipids hypothesis [4] notes that the oxidation of phospholipids bound in the LDL particle, and especially phospholipids containing arachidonic acid, are inflammatory. In the presence of such oxidized LDL, HDL is found to be anti-inflammatory. What starts the inflammation is not clear, but an early step is entry of monocytes from the blood into the artery wall [5], possibly recruited by oxidised LDL, or by Cholesterol peroxides, which are particularly inflammatory.. The monocytes then become macrophages and generate cytokines from arachidonic acid. Apolipoprotein B in LDL becomes tagged with a product of lipid oxidation, and is then accumulated by cells in the artery wall. Lipoxygenase-negative mice have “significantly” less atherosclerosis. (Hmm!). However, in humans, vitamin E and other antioxidants have proved clinically ineffective in combating atherogenesis. It seems that the growing plaque can do one of three things: [a] regress, [b] stabilise, [c] rupture. Even the ruptured plaque can stabilize, but leaving the artery with a restricted lumen [5].

Accounts emphasise different aspects but none are clear on the first step. Does dietary cholesterol get oxidised by oxygen radicals generated in the intimal layer of the artery wall? Nor is it clear why the body generates all this fuss; is the inflammation and the plaque protective?

Isoprostanes (peroxidized products of arachidonic acid and other polyunsaturated fatty acids that participate in the perception of pain) flag the presence of oxidative stress. They are found in the urine, particularly of smokers. So, smoking correlates with increased oxidative stress, perhaps by blocking the flow of electrons to oxygen, for smoke contains both CO and CN-.

Is there a feedback loop here? with the ischaemia causing radicals, which then attack the intima and cause further occlusion?

Friday, 15 September 2017

I recently received a small yellow padded envelope by second class ‘Royal Mail Signed ForTM’ delivery. I was out when it was first delivered and I had the choice of going down to the sorting office in the town some miles away, or requesting that the package be re-delivered on the next available day. I chose the latter as the least inconvenient; I had only to stay in the house till the package arrived.

It was addressed to “The Manager”, but I signed my usual squiggle on the little electronic box the postie held out for me. Inside there was nothing. Figuring that the operation would cost the sender over £1 (including envelope and franking), I began to wonder what the purpose was. I went online to search for similar experiences.

One blogger posted the suggestion that the hidden reason was harmless enough, simply that of inflating apparent turnover of online sales to impress clients or competitors. Well, I saluted the ingenuity of both the poster and the blogger, for I had not come up with any cogent explanation of my own (not that I had tried that hard).

Then I came across the suggestion that the scam is more sinister and works as follows. An innocent online customer buys and pays for an item and is given the ‘tracking number’ (in this case KK461028710GB). The scammer posts an empty package to an arbitrary addressee who innocently signs for the package before opening it and finding it empty. The ‘mark’, waiting in vain for his item, eventually checks with Royal Mail who tell him (to his surprise) that the item has been delivered and shows the irrelevant signature. No redress!

The scammer no doubt trusts that the innocent addressee, as he is little affected, will forget the incident. In order to frustrate that expectation I post this here and invite comments.

Sunday, 10 September 2017

A year and a half ago, the launching of DiEM filled me with hope, particularly in the context of the British referendum. Since then DiEM25 seems to have slipped off the main stage, which is a pity. I wish I could help it re-find its momentum.

One way of seeing the problem is when we hear Yanis Varoufakis describe his confrontations with the central powers of the EU. They met, talked, listened. He left. They did nothing. My first analysis was that they did not understand. Indeed, I found it very hard to repeat the argument to myself; about how it is all Germany's fault, so stubbornly bent on recycling money so that the Greeks can go on buying Mercedes cars. My second analysis is that Yanis does not understand. Oh yes, he understands the economics; but the crux, the movable fulcrum, the point in the argument against which a popular movement might push and win — has he identified that?

Martin West thinks the single currency is a mistake. No single interest rate can suit both Germany and Greece. Put another way: how does it work in the USA, and how can Ecuador and the USA both use the same currency? I believe there is an understanding in the USA that federal money must be returned to poor states if they are going to be kept in the union. I do not know how. There may, in that complex and subtle constitution, be a degree of political integration that is still missing in Europe. Or is it just the common language? But perhaps we do agree that something needs to be done about the Euro Currency Union.

Yanis Varoufakis suggests there is a democratic deficit? Before the Brexit Referendum, that sounded like a promising slogan, but we now see what a mess is made if complex issues are decided by simple people. It is not obvious to me that it is democracy that we lack. I believe it is education.

Can Europe be 'cured' by allowing more power to the EU parliament? I doubt it. Or by curbing the EU civil service? Possibly. But we have to recognize that the origin of the EU depended on the dreams of a very few people; integrated Europe is not the product of a popular dream. Only by imbedding the guiding force in a hidden and inaccessible committee was it possible to get the project of a united and inter-dependent Europe off the ground. It is true that we pay lip service to democracy, but I doubt we really believe in it, except to rally forces against flagrant corruption. I do not think we are quite there yet; I mean the corruption is not flagrant enough; people are not convinced that revolution would improve their situation.

I think the Pro-Europe lobby finds its greatest traction at present by showing that the EU is protecting workers rights, clean beaches, fish-stocks and, by instituting uniform production standards, is allowing economies of scale. These are the tangible and practical benefits of integration. For me, and for a considerable fraction of Europeans, there is some appeal in the thought that United Europe could be (would be) a great power. Britain being part of Europe would allow Britain to effect some control in world affairs.

Arguably the most depressing sign at present is the resurgence of nationalism. The British seem to think they are special (which may be true), but special in a ‘good’ way; this, to any travelled person is clearly a delusion.

Yanis Varoufakis believes that right-minded people will spontaneously support socialism. In Britain, they do not; or they are too few. He suggested that all businesses subvert a fraction of their profits towards the public purse, to illustrate the principle that wealth is generated by a combination of capital and labour**. That suggestion sounds drastic and risky, and unlikely to garner mass public support. (Though admittedly, it is little different from our widely accepted but as widely resented corporation tax.)

Friday, 25 August 2017

A year or two ago (Feb, 2014) I heard Professor Ian Young, (Director of the Centre for Public Health, Queen’s University Belfast) give the Albert Latner lecture at Newcastle University on “My cholesterol — why is it so high?”. It was a most frustrating affair. Why?The man presented no chink of doubt, he missed some serious points, and he spoke like a missionary, or a man whose salary is largely augmented by the manufacturers of statins. We must all take statins from infancy up (we were told). He kept saying that a 1mM(*) drop in total cholesterol causes a 25% lowering of risk of vascular event; but, while his curves showed a steep line of correlation for 40 year olds, it was an almost flat line for 80 years. (So for me there is practically no benefit).

But a more important point: In no case was the vertical axis on any of his graphs ‘General health’; he was only talking about ‘Rate (or risk) of vascular event’. It has been said that "to a hammer, everything looks like a nail", and to a cardiologist the only objective is to lower the risk of a ‘vascular event’. What about the adverse side-effects; the muscle pains, and increased risk of diabetes (both of which Young conceded), Alzheimer’s, ALS, and Parkinson’s (which were mentioned by Stephanie Seneff; https://people.csail.mit.edu/seneff/)?

Cholesterol is essential. Ian Young correctly remarked that blocking the synthetic pathway at HMGCoA synthase (which is what statins do), will indeed cause a shortage of cholesterol and lead to scavenging pathways and the relocation of existing cholesterol. If the scavenged cholesterol is from coronary plaques, well-and-good; but what if it is scavenged from brain myelin or muscle cell membranes (as emphasised by Stephanie Seneff)? And what about ubiquinone and dolicol, which are also essential and also on the pathway blocked by statins (as emphasised by Stephanie Seneff )? If there ARE INDEED adverse side effects of statins, it is easy to see why!

So the clinical debate should be about the side effects versus benefits. I heard a paper in a Glasgow Heart meeting in the late 1990s which concluded that for over 40 year olds (or was it over 50?) the OVERALL benefits of statins do not outweigh the OVERALL damage. I was impressed (staggered, indeed) at the failure of the clinical cardiologists to see that this—if true—trumped the undenied fact that statins lower cardiovascular risk.

In 2014, aged 72 but in perfect health, I concluded I was certainly not going to take statins. I did not feel I needed them. And whether or not I should lower blood cholesterol there is something too utterly daft about poisoning myself at great expense in order to achieve that; and simply to switch from a healthy death from a coronary to a lingering death from mental, muscular and neurological decay. If I were under 40 and had familial hypercholesterolaemia (**), I think I would try diet, red-wine, and niacin (e.g. brewer’s yeast) before I tried statins.

Professor Ian Young talked away about nuts, expensive margarine, salt, exercise, the ‘J’-curve for alcohol, etc. But he conceded that only 10% of our cholesterol comes from diet. So, surely the question is why do we MAKE too much? What regulates the synthetic pathway? [***] Does alcohol in excess of 2 units per day, or smoking, etc, up-regulate the synthetic pathway, or affect the partitioning between pools of cholesterol, e.g. by enhancing oxidative damage? What is the rôle of lipid oxidation (briefly mentioned by Young)?

Young pointed out that HDL-cholesterol is “good”; that low ‘cardiovascular risk’ correlates with higher HDL (in the 1 – 2 mM range, independently of LDL or total Ch.); in fact high HDL-Ch is 10-fold healthier than low HDL-Ch (while low LDL-Ch is only 3 times healthier than high LDL-Ch); the best predictor of heart disease is therefore the ratio LDL/HDL, the next best is HDL, the least good is LDL or total blood cholesterol. So, further good questions would be: what determines partitioning of cholesterol between the various ‘pools’ of cholesterol (HDL, LDL, cell membranes and atherosclerotic plaque, its locus operandi (where it is needed, in muscle and nerve membranes), and its locus morbidus (i.e. coronary plaques where it appears to be deleterious)? Also, what is the rôle of lipid oxidation in affecting the partitioning? Presumably the HDL particle is picking up and re-locating cholesterol and is wholly good. But it is 'HDL-cholesterol' that is measured, so we do not know if the HDL is largely unloaded or nearly full; the latter giving the impression of plenty of HDL particles, but actually being nearly useless as a scavenger. There is a route for elimination of lipid, lipid-cholesterol-ester and cholesterol which involves liver, bile and gut. Guessing here, and maybe naively, but is it damaged (e.g. oxidized) fat/cholesterol that is eliminated, rather than merely surplus? So, there are plenty of unanswered questions.

Perhaps the coronary plaques are, in a wider sense, beneficial. After all, they protect us against suffering from Alzheimer’s disease, and a lingering death! What, in any case, are the evolutionary benefits (to the genes) of surviving beyond the age of 70? The benefits must be very small and may be negative; a little ‘grandparenting’ perhaps, and some dubiously relevant ‘advice’; but does that pay for the food and the space?

(* mmol total cholesterol per litre blood)(** There are many types of familial
hypercholesterolaemia; the most common by a factor of 2 is a defective
LDL-receptor, which presumably hoicks LDL particles out of the
circulation and into some (presumably) removal pathway.)(*** My erstwhile colleague Loranne Agius suggested that the ingestion of excess carbohydrate feeds into fat production in the liver which requires cholesterol for its excretion.) PLEASE COMMENT

Tuesday, 20 June 2017

BT help, BT — help!

I wonder if readers will think I am paranoid in seeing a possible malfeasance in the following story.

I get a crescendo of letters and emails from my Internet Service Provider (ISP, namely BT) suggesting I upgrade to 'Infinity Broadband'. (I ignore these as the 15 megabit/s download rate is sufficient for my needs). The last email from BT said they would waive the conversion fee of £50 if I decided to upgrade before 23rd June. Then my hub becomes disconnected from the internet for two or three hours on Sunday afternoon, which is distressing because we spent several wasted hours trying to transfer money in Mexico. Then we are connected again, till Monday noon. Then disconnected again during Monday afternoon when the Mexican banks become open (BST+6hrs). I phone the helpline and a young welsh woman spends some 45 minutes “running tests” all of which come up negative. So BT say there is “no fault” and therefore no way they will replace or upgrade my hub free of charge.

The only remedies she could offer were (a) to replace at a cost of £50 the hub(1) I currently have and remain on the same monthly contract as at present, or (b) upgrade ‘free' to a new hub(2) and contract at a considerably higher monthly cost, or (c) a mixture of the two whereby I pay £20 to come onto a moderately raised monthly rate.

I say there certainly is a fault; and the service, for which BT and I are contracted, is failing, with no apology from BT and no mention of compensation. Not only that, but BT has failed to find the fault, and thereby wasted another hour of my time.

Wednesday, 7 June 2017

Is there an honourable case against Proportional Representation?

It struck me recently, that there would have been no need for a referendum if we had had proportional representation (PR) in the House of Commons. So, who is against PR? And why? One prominent Tory MP is recorded as saying: “The principle argument against the present system is that it is not fair – it is not a proportional system. However, proportional representation is a narrow concept. The ‘proportionality’ relates only to the relationship of votes to seats and not to the proportionality of power. Under PR, 10% of the votes are designed to produce 10% of the seats, but not necessarily 10% of the negotiating power in the House of Commons. Indeed, a party with 10% of the seats may be in a position to wield disproportionate negotiating power.” She seems to be raising two objections to PR; that it is a “narrow concept”, and that while the votes may be distributed fairly under PR, the power is not. I do not understand the first point, unless it is intended as a summary of the second point. The second point is familiar. Politician on left and right have long been aghast at the thought of centre parties holding “the balance of power” whether under a Tory minority government or a Labour. But surely this is a relatively simple error. Suppose the House of Commons contains 300 Tories, 280 Labour, 30 Lib-Dem. Suppose, on a Tory motion, Lib-Dem and Labour MPs vote (in a principled way) against, and the motion is therefore defeated. The power that defeated the motion does not reside in the Lib-Dem portion of the opposition, but in all 310 opposers ! The motion is defeated only if there are more MPs against the motion than for; each MP counting for one vote. Surely I have said enough! My protesting Tory MP seemed worried that centre parties in a proportional parliament have more power than extreme parties. But that is also nonsense isn’t it? No one can seriously advocate disenfranchising the moderate middle merely to give the extremes a chance to govern! It is a lunatic suggestion. Anyone who is against the moderate voices being in the majority is up against an immutable natural law — the bell-shaped curve of the "Normal Distribution" shows that the majority ARE in the middle. I hope no one will oppose PR on foolish grounds. I have heard other objections to PR.Some people (arguing against PR) say, “Look at Italy”. To which I would reply “Look at The Netherlands”. Perhaps we should consider the possibility that the combined opposition unanimously wanted to vote strategically, playing games with parliament and the whole process of government. But that argument is answered by a number of considerations: such behaviour defeats good government, the perpetrators would be punished at the next election, the same game could eventually be played against them. The concept of parliament, and democracy itself, is based on the assumption that MPs do not play silly games. It is sometimes remarked that the present flip-flop system makes for large majorities and “decisive” government. But that is surely the DISADVANTAGE of the present system, and by no means its strength? There is little virtue in being decisive if you are going against the wishes of the country; and none if you are plain wrong. When one party holds a large majority for 5 years, legislation is not tested. Furthermore, the backbench andopposition MPshave little to do. Add to that the devastating effect this flip-flop system has on morale in the country; the people cease to vote, for they see that their votes are not counted, and the MPs overuse their privileges. Perhaps we should consider also the problem of stasis; getting stuck on the fence. But this also is to underestimate the good sense of the House? Ocean liners do not routinely run aground for inability to decide whether to pass to the left or right of an obstacle.) Proportional Representation is not a new concept. Many (if not most) countries have adopted it. The referendum of May 2011 was not about PR; it was a choice between staying with the present system or changing to the 'Alternative Vote' system which is not proportional, has few advocates, and few users.The ‘First Past the Post’ system favours two large parties, and large parties cynically favour it in return. I hope no one will oppose PR on dishonourable grounds. But perhaps I have missed something.Yours sincerely, Cawstein(South Northamptonshire.)

Tuesday, 23 May 2017

Nocturne in F minor (Op 48, No. 2)
—Frédéric Chopin(1810 – 1849)

A nocturne is supposed to be inspired by, or
evocative of, the night, or at the very least played at night. Mozart wrote 'notturnos' for mixed wind and strings, but the Nocturne as a short piano piece
was more-or-less invented by the Irish pianist/composer John Field (1782 – 1837).However the form was made his own by
Chopin who, between 1830 and 1846, wrote 21 of these characteristically short,
moody, pieces. This nocturne was written in 1841 and published the following
year. It is marked Andantino.

12 Etude Opus 25——— Frédéric Chopin(1810 – 1849)

Chopin wrote 27 Studies in all; 12 in the opus
10 set published in 1832, and 12 in this set written over a space of 4 years
but published in 1837. They are, of course, studies for the establishment of
fundamental piano technique, and many piano virtuosi have composed studies for
that purpose, but these by Chopin rise far above the majority in artistic
merit, and can be seen as compositional studies over and above their technical
role. Chopin himself performed this opus 25 set at a concert, greatly
impressing Robert Schumann. Except that 2 and 11 are both in A minor, each is
in a different key.

++++++++ Interval ++++++++++++

Rhapsody Opus 79/1 —— Johannes Brahms (1833 – 1897)

The two " Klavierstücke " of opus 79
were written in 1879 at the summit of his career. They were dedicated to his musical
friend Elisabeth von Herzogenberg (herself a composer), and it was she who
suggested the slightly pompous renaming of them as 'Rhapsodies'. This No. 1
Rhapsody is like a compressed sonata; the Agitato outer sections (in
'sonata-form') are in B minor, but they surround a more lyrical section in B
major.

Nutcracker Suite — Pyotr Tchaikovsky (1840-1893)/Mikhail Pletnev

This is a piano transcription made by our
contemporary Russian virtuoso pianist and conductor Mikhail Pletnev (1957 - )
of Tchaikovsky's Suite for Orchestra which lasts 20 minutes. The original
ballet of 1892 was based on a story by ETA Hoffmann and is in two acts. In Act
1 the characters are human (adults and children) and the toys are toys; in Act
2 they are fantasy — the toys coming to life. There are 23 sections in the
ballet, all with evocative titles like 'Decoration of the Christmas Tree',
'Children's Gallop and Dance of the Parents','Waltz of the Snowflakes', in Act 1; while in Act 2 taking
place in the Land of the Sweets there are: Chocolate (Spanish dance), Coffee
(Arabian dance), Tea (Chinese dance), Waltz of the Flowers,Pas de deux (Sugar-Plum fairy and her
Chavalier),a Tarantella, the
famous Dance of the Sugar-Plum Fairy, and a Final Waltz and 'Apotheosis'. In
Pletnev's version there are 7 pieces:March, Dance of the Sugar Plum Fairy, Tarantella, Intermezzo, Trepak
(Russian Dance), Tea (Chinese Dance), Pas de Deux.

When Prokofiev was in Chicago in 1921 he was
commissioned to write an opera. Fortunately he had a draft libretto for a
satirical opera in his bag. Knowing as little English as the Americans had
Russian, the opera came out first in a French version – "L'amour des trois oranges". The
critics were initially doubtful ("The
work is intended, one learns, to poke fun. As far as I am able to discern, it
pokes fun chiefly at those who paid money for it."). Prokofiev
prepared a 20 minute orchestral suite derived from the music (Styled Opus 33
bis); and from that himself prepared this Scherzo and March for solo piano (Op.
33 tert).

Piano Sonata A minor, Op. 28 ––––
Sergei Prokofiev (1891 – 1953)

Prokofiev composed his first opera when he was
9. His father died in 1910 and with him financial security, but the 19 year old
son was already becoming known as a composer, albeit in a very 'modernist',
polytonal, discordant, vein.Prokofiev's 3rd piano sonata was 10 years in the making; it
was published in 1917, the year of the Russian Revolution (Feb), and
Prokofiev's departure for America (May). It is a short (8 min) work in one
movement, and illustrates Prokofiev's interest in departing from the norms of
the romantic school; in shock, dissonance, harsh clusters of notes, and dynamic
surprises. (Apparently, he was throughout his life an excellent chess player.)

Saturday, 13 May 2017

String Quartet in D, K. 575 —— Wolfgang Amadeus Mozart (1756 — 1791)

i. Allegretto; ii. Andante; iii. Menuetto (Allegretto); iv Allegretto

In April we heard Mozart's Quartet No. 22 in B flat major
(K589, Prussian No. 2); today its predecessor, No. 21, the first of the
so-called 'Prussian Quartets'. In April 1789, Mozart's wife claiming illness
and needing a spa cure (where however she flirted to Mozart's distress), left
Mozart desperate for money. Hope came when Prince Lichnowsky, an aristocratic
pupil, offered to take him to Berlin and present him to King Friedrich Wilhelm
II (himself an amateur cellist). He came back to Vienna intending to write 6
quartets for the King and 6 'easy' piano sonatas for his daughter Princess
Frederike. Of the latter, only one was written — Mozart's last piano sonata. Of
the quartets, Mozart wrote only 3. Somewhat neglected, these quartets are
overshadowed by his earlier 'Haydn' quartets and the later quintets. Some of
his contemporaries got the impression that Mozart wrote with a facility
bordering on flippancy for he would write out the score without errors while
talking to friends, but others insisted that he spent much of the night at the
piano, and it was only his extraordinary memory that enabled him to write the
fair copy at speed. A distinctive feature of all 3 'Prussian' quartets is the
prominent and interesting cello part, intended for the king himself to play. In
this, the first of the set, 3 of the 4 movements are marked allegretto ('mildly cheerful' ?). The outer
movements are in D major; the andante
second movement is in A, the minuet (in D) has a trio section that swithers
between D and G.

String Quartet No. 2, (Op. 17) —— Béla Bartók (1881 – 1945)

i. Moderato;ii. Allegro molto capriccioso;iii. Lento

At the age of 21 Bartók, travelling abroad as a virtuoso
pianist, was stimulated by Strauss's Zarathustra
to try his hand at composition (Kossuth
in 1903). In 1904, hearing a nanny sing a folk song he was stimulated to take
up the collecting and study of Folk Music as his main preoccupation and life's
work, with only occasional diversion into composition: the 1st
quartet (1909), an opera Bluebeard's
Castle (1911), 2nd quartet (1917), the ballets Wooden Prince (1916), and Miraculous
Mandarin (1919). In 1909 the 28 yr old Bartók married 16 yr old Marta. By
then, he was living in Budapest as professor of pianoforte at the Royal Academy
of Music (where one of his pupils was Sir Georg Solti). The First World War was
a relatively peaceful time in Hungary. For Bartók and his colleague, great
friend and fellow collector Kodály, it meant that they had to give up their
travelling abroad collecting folk songs onto wax cylinders and return to
Hungary; turmoil came with Hungary's Soviet revolution after the war. So Bartók
spent most of the war simultaneously writing the Wooden Prince and his 2nd quartet; both showing the influence of
Debussy. Bartók apparently described the first movement as being in sonata
form, the second as "a kind of rondo" and the third as
"difficult to define" but possibly a sort of ternary form (Wikipedia). It is not in his 'mature' style, which developed only in the
twenties and thirties.

This quartet, composed in 1827 when Mendelssohn was 18 years
old, is actually his first, as Opus 12 (though called Quartet No. 1) was
written two years later. It astonishes the listener with its assured mastery of
the medium, and its bold originality; but then we remember that he wrote his
superb String Octet (1825) two years before that. Many musicologists have compared
Mendelssohn's opus 13 with Beethoven's late quartets, the last of which, though
not performed in public till 1828 was published in September 1827 (Beethoven
died March 1827). (See e.g.: http://www.gresham.ac.uk/lectures-and-events/mendelssohn-quartet-in-a-minor-op-13.)While most contemporaries regarded
these late Beethoven quartets as flawed, and even 'horrible', the young
Mendelssohn must have obtained and studied the score in the weeks before
writing his opus 13. An easily conceded but trivial similarity between older
and younger master is that the final movement of Beethoven's last quartet (Op.
135) opens with a musical motif under which Beethoven wrote "Muß es sein?" ("Must it be?"),
while in the last 5 bars of the opening adagio, adolescent Mendelssohn quoted
the "Ist es wahr?" motif
from a song he had previously written (of which the words run "Is it true,
is it true that you are always waiting for me in the arboured walk?"). But
the one utterance is a disturbed, existential question, while the other
expresses the uncertainty and excitement of a youthful romantic yearning. So
differ also the works.

Monday, 1 May 2017

Four Impromptus, (Op. 90), D. 899 ―Franz Schubert (1797 – 1828)

These 4 impromptus were composed in 1827 (a year before
Schubert's untimely death), and published the same year; the first half of a
set of 8. In that year Schubert composed, besides these exquisite short piano
pieces, yet another failed opera (The
Count of Gleichen), a superb German Mass, the E flat piano trio and the
sombre song cycle "A Winter Journey".
A year of great happiness and sadness; a torch bearer at Beethoven's funeral,
letters from 3 publishers asking to publish his compositions, a holiday in
Upper Austria (said by Hutchings to be "perhaps the most happy time
Schubert had ever known outside Vienna, or in it"). The first Impromptu, in C minor, is
a set of variations on two themes; both slow. It ends peacefully in the major.
The second, in E flat major,
is in ternary form, but with a B-like coda (ABAB'). The A section is a
moto-perpetuo of running triplets for the right hand; the contrasting B section
drops into a minor key and, approaching the return, it intriguingly combines
hints of the running triplet figure. The third,
a peaceful, lyrical, reassuring piece in G flat major (6 flats), was reissued
30 years later by the same publisher in G major (1 sharp; for amateur
players?)The fourth Impromptu, in A-flat major, is perhaps the most
famous of all Schubert's piano compositions. Its opening consists of cascading
arpeggios in the right hand, nowadays usually trivialized by being played too
fast in an attempt to bring out the left hand melody. It begins transiently in
A-flat minor, though this is written as A-flat major with accidentals. It is in
ternary form (ABA) with a calmer middle section. Was this set a sonata taken
apart? Probably not, as Schubert numbered his next 4 impromptus 5,6,7,8.
However, these 4 impromptus played in this order fit nicely together in mood
and key.

Three Piano Pieces, (Op. 90), D. 946 ――Franz Schubert (1797 – 1828)

Schubert died on 19th November 1828. Between
March and the beginning of November he wrote: the C major String Quintet, 3
piano sonatas, 2 piano duets (includning the profound Fantasie dedicated to the young countess Caroline Esterhazy), these
3 Klavierstücke, The Shepherd on the Rock, the Schwannengesang
songs, and 3 pieces of church music. It was doubtless the fugal writing of the
latter that prompted Schubert to turn up on 4th Nov with friend Lanz
on the doorstep of Simon Sechter's house for lessons in counterpoint. He missed
the second lesson on 10th, and took to his bed 4 days later,
fiddling still with the unsuccessful opera The
Count of Gleichen. So, a year that saw written much of his sublimest music.
These 3 Klavierstücke, written in
May, were published (by Brahms) in 1868. It seems likely that there were to be
4, but it is not clear whether they were to be Impromptus or Moments Musicaux,
nor even that they were conceived as a set. They are more complex in structure
than the preceding set of impromptus (e.g. the 1st is in what could
be called compound ternary form: A,B,A',C, D,E,A,B,A',C), they favour remote
keys (e.g. 6 and 7 flats), continuous triplets and repeated semiquavers or
tremolo effects; all typical of late Schubert. The firstis in E♭ minor and marked Allegro Assai. The second, in E♭ major is Allegretto.
The third is an Allegro in C major, in which it sounds
as though the left hand is behind the beat, but it is really the right hand
that is before the beat.

Sonata in D major, (Op. 53), D. 850 ――Franz Schubert (1797 – 1828)

After Schubert's despair in 1824, 1825 was a relatively
happy year. He was solvent with Esterhazy guilders, and becoming known to
publishers and the musical world of Vienna. He spent from May till September in
the ravishing countryside of upper Austria with the retired opera singer Vogl
who was a native of that area, moving from place to place, singing and charming
as they went, welcomed and dined by the local big-wigs, and charmed in their
turn by the young ladies. But it was not all sight-seeing and letter-writing,
for Schubert composed his Great C major (9th) Symphony, the Walter Scott songs
(which include his Ave Maria), and
this D major sonata. For the last 3 weeks, paid for by a well-wisher, he and
Vogl stayed at the famous health spa of Bad Gastein (therapeutically
investigated by Paracelsus 300 years earlier); so this is called the Gasteiner
Sonata. Schubert's composer brother Ferdinand, when offering to sell it to
Diabelli after Schubert's death, distinguished it as a Grand Sonata; perhaps on
account of its length. It is, however, relatively light hearted, and in many
passages has an improvisatory feel. The 1st movement is vigorous; the long
andante (in A major), dreamy rather than sombre or painful; the scherzo,
rousing, with a sharply contrasted sweet trio section; the rondo almost cheeky
in the nursery-like simplicity of its recurring theme.

About Me

My Cawstein profile shows me struggling to understand politics, economics, and occasionally philosophy, commenting on the misuse of the English language and other perceived follies gaining currency in our times

Of course, this Cawstein only emerged when the web itself emerged. Before that there was neither the means of developing these characteristic ideas, nor the time. I suffered as a child the constraint of having to go to school. Then there were 45 years of disciplined application to a career in academic biochemistry (where my contributions lay in bioenergetics and membrane transport, chiefly in bacteria and mitochondria).